Enhanced Renal Vascular Responsiveness to Angiotensin II and Norepinephrine: A Unique Feature of Female Rats with Congestive Heart Failure

0511914 - FGÚ 2020 RIV CH eng J - Journal Article
Krátký, V. - Kikerlová, S. - Husková, Z. - Sadowski, J. - Kolář, František - Červenka, L.
Enhanced Renal Vascular Responsiveness to Angiotensin II and Norepinephrine: A Unique Feature of Female Rats with Congestive Heart Failure.
Kidney & Blood Pressure Research. Roč. 44, č. 5 (2019), s. 1128-1141. ISSN 1420-4096. E-ISSN 1423-0143
R&D Projects: GA MZd(CZ) NV18-02-00053
Institutional support: RVO:67985823
Keywords : heart failure * female * aortocaval fistula * angiotensin II * norepinephrine
OECD category: Cardiac and Cardiovascular systems
Impact factor: 1.898, year: 2019
Method of publishing: Open access
https://doi.org/10.1159/000502379

Background/Aims: We found recently that the aortocaval fistula (ACF)-induced heart failure (HF) results in higher mortality in female than in male rats. Possibly, the development of renal dysfunction in the females, unlike in males, is associated with altered renal vascular responsiveness to angiotensin II (ANG II). Methods: Five or 20 weeks after ACF creation (compensated and decompensated HF, respectively), we assessed renal blood flow (RBF) responses to intrarenal administration of ANG II, norepinephrine (NE), and acetylcholine (Ach) in female ACF and sham-operated rats. Results: In ACF females, ANG II decreased RBF more than in healthy animals, unlike with earlier published data in male ACF rats that responded similarly. Also, NE decreased RBF more in female ACF rats, whereas Ach increased RBF to the same extent in female ACF and sham-operated rats. RBF responses to intravenous administration of NE and Ach were almost identical in female and male ACF rats. Conclusion: Female ACF rats studied at the onset of HF decompensation reveal, in contrast to male rats, enhanced renal vascular responsiveness to both NE and ANG II. When associated with the demonstrated increased intrarenal ANG II and NE concentrations, such hyperresponsiveness might promote the development of renal dysfunction and accelerate HF decompensation.
Permanent Link: http://hdl.handle.net/11104/0302148